In a 67-year-old man with multiple myocardial infarctions in the past, the use of oral verapamil for control of angina pectoris was followed by the appearance of two previously undiagnosed abnormalities, namely, a dual-pathway AV node conduction pattern, and paroxysms of AV nodal reentrant tachycardia precipitated by premature ventricular beats (PVB). It is probable that the differential effects of verapamil on the fast and slow AV node pathways, and the interplay of PVB with its concealment within the AV node, created the necessary circumstances in the AV node to precipitate the tachycardia. Observed off verapamil over several months, the patient remained in normal sinus rhythm but continued to have numerous premature ventricular beats (PVB's). Nevertheless, neither the clinical electrocardiographic features of dual-pathway AV node conduction nor the AV nodal reentrant tachycardia could be found. The proarrhythmic effect of verapamil and its ability to provoke the very arrhythmia against which it is most effective are of particular interest in view of a similar behavior exhibited by the Class I antiarrhythmic agents.